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Description of key information

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential

Additional information

There are no data on the toxicokinetics of dichloro(dimethyl)silane.

The following summary has therefore been prepared based on predicted and measured physicochemical properties of the substance itself and its hydrolysis products and using this data in algorithms that are the basis of many computer-based physiologically based pharmacokinetic or toxicokinetic (PBTK) prediction models. Although these algorithms provide quantitative outputs, for the purposes of this summary only qualitative statements or predictions will be made.

The main input variable for the majority of these algorithms is log Kow so by using this, and other where appropriate, known or predicted physicochemical properties of dichloro(dimethyl)silane or its hydrolysis products, reasonable predictions or statements may be made about their potential absorption, distribution, metabolism and excretion (ADME) properties.

Dichloro(dimethyl)silane hydrolyses very rapidly in contact with water (half-life 0.2 minute at pH 4, 0.3 minute at pH 7 and 0.1 minutes at pH 9 and 1.5°C) producing dimethylsilanediol and hydrogen chloride. Relevant human exposure would be via the inhalation or dermal routes. Relevant inhalation exposure would be to the hydrolysis products (hydrolysis would occur rapidly when inhaled, even if a mixture of parent and hydrolysis products were present in air). The substance would also hydrolyse rapidly in contact with moist skin. The resulting hydrogen chloride hydrolysis product would be severely irritating or corrosive and this results in the parent substance being corrosive and this is the critical health effect for the registered substance.

Potential systemic exposure to hydrogen chloride is not discussed.



Significant oral exposure is not expected for the corrosive parent substance, dichloro(dimethyl)silane. However, oral exposure to the hydrolysis product dimethylsilanediol is potentially possible via the environment.

When oral exposure takes place it can be assumed, except for the most extreme of insoluble substances, that uptake through intestinal walls into the blood occurs. Uptake from the intestines can be assumed to be possible for all substances that have appreciable solubility in water or lipid. Other mechanisms by which substances can be absorbed in the gastrointestinal tract include the passage of small water-soluble molecules (molecular weight up to around 200) through aqueous pores or carriage of such molecules across membranes with the bulk passage of water (Renwick, 1993).

Although DMSD has a predicted water solubility of 1E+06 mg/l the concentration in aqueous solution is likely to be limited by condensation reactions at loadings above approximately 1000 mg/l. The prediction is however considered valid for use in toxicokinetic modelling because it is adequate to describe the hydrophilicity of the substance and hence the partitioning behaviour. Therefore, if oral exposure did occur, dimethylsilanediol with its predicted water solubility and a molecular weight of 92.17 clearly meets these criteria so should oral exposure occur then systemic exposure is very likely.

In a repeat dose oral study (Dow Corning Corporation, 2009) with the hydrolysis product, dimethylsilanediol, pathological effects were recorded indicating absorption of substance-related material.


An in vitro dermal absorption study using human skin showed a dermal absorption for the hydrolysis product, dimethylsilanediol, of 11.4% following a 24 hour exposure period. It also showed that approximately 60% of the applied dose evaporated from the application site.

Since dichloro(dimethyl)silane is corrosive to the skin, damage to the skin might result in some increased penetration of the hydrolysis product.

There are no reliable studies to check for signs of dermal toxicity. Skin irritation/corrosion studies did not show any signs of systemic toxicity.


There is a Quantitative Structure-Property Relationship (QSPR) to estimate the blood:air partition coefficient for human subjects as published by Meulenberg and Vijverberg (2000). The resulting algorithm uses the dimensionless Henry coefficient and the octanol:air partition coefficient (Koct:air) as independent variables.

Using these values for dimethylsilanediol results in a blood:air partition coefficient of approximately 1.6E-02:1 meaning that if lung exposure occurred uptake into the circulatory system would be unlikely. However, the high water solubility of dimethylsilanediol suggests that it could be dissolved in the mucous of the respiratory tract lining, so it may be passively absorbed from the mucous, increasing the potential for absorption.

As with dermal exposure, damage to membranes caused by the corrosive nature of the hydrogen chloride hydrolysis product might enhance the uptake. Acute inhalation studies (Dow Corning Corporation, 1997 and 1987, BRRC, 1982) showed local signs of irritation but no definitive systemic effects.


For blood:tissue partitioning a QSPR algorithm has been developed by DeJongh et al. (1997) in which the distribution of compounds between blood and human body tissues as a function of water and lipid content of tissues and the n-octanol:water partition coefficient (Kow) is described. Using this value for dimethylsilanediol predicts that, should systemic exposure occur, potential distribution into the main body compartments would be minimal.

Table 1: Tissue:blood partition coefficients


Log Kow
















Dichloro(dimethyl)silane is rapidly hydrolysed to dimethylsilanediol and hydrogen chloride in the presence of moisture. Most if not all of this will have occurred before absorption into the body. There are no data regarding the metabolism of dimethylsilanediol. Genetic toxicity tests in vitro with the parent substance, dichloro(dimethyl)silane, showed no observable differences in effects with and without metabolic activation.


A determinant of the extent of urinary excretion is the soluble fraction in blood. QPSRs as developed by DeJongh et al. (1997) using log Kow as an input parameter, calculate the solubility in blood based on lipid fractions in the blood assuming that human blood contains 0.7% lipids.

Using the algorithm, the soluble fraction of dimethylsilanediol in blood is >99% meaning that once absorbed it would be likely to be eliminated via the kidneys in urine and therefore accumulation is unlikely.


Renwick A. G. (1993) Data-derived safety factors for the evaluation of food additives and environmental contaminants. Fd. Addit. Contam. 10: 275-305.

Meulenberg, C.J. and H.P. Vijverberg, Empirical relations predicting human and rat tissue:air partition coefficients of volatile organic compounds. Toxicol Appl Pharmacol, 2000. 165(3): p. 206-16.

DeJongh, J., H.J. Verhaar, and J.L. Hermens, A quantitative property-property relationship (QPPR) approach to estimate in vitro tissue-blood partition coefficients of organic chemicals in rats and humans. Arch Toxicol, 1997. 72(1): p. 17-25.